ArticleArteriosclerosis, thrombosis, and vascular biology2025
Nitrosation of CD36 Regulates Endothelial Function and Serum Lipids.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Endothelial nitric oxide signaling in cellular and systemic metabolism.Redox biology · 2026Review
- Guidelines for evaluating endothelial function in vascular tissue.American journal of physiology. Heart and circulatory physiology · 2026Review
- Endothelial Cell Regulation of Lipid Uptake During Feeding and Fasting.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Global knockout of VEGFB improves lipoprotein lipase activity leading to an improved lipid profile during diabetes.Frontiers in pharmacology · 2026Article
- Lipid overload meets S-palmitoylation: a metabolic signalling nexus driving cardiovascular and heart disease.Cell communication and signaling : CCS · 2025Review
- Just Say NO to CD36 Expression: A Regulatory Pathway With Implications in Many Chronic Diseases.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Fatty Acid Transporter CD36 Promotes Ox-LDL-Induced Senescence of Vascular Endothelial Cells in Preeclampsia.Journal of inflammation research · 2025Article
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22 authors.
Funding
Abstract
backgroundDuring obesity, endothelial cells (ECs) become lipid laden, leading to endothelial dysfunction. We tested posttranslational modification on cluster of differentiation 36 (CD36) that may regulate EC lipid accumulation.
methodsWe used an EC-specific Cav1 (caveolin-1) knockout mouse, nitrosation and palmitoylation assays, and whole animal Nγ-nitro-l-arginine methyl ester administration to examine blood lipids.
resultsEC-specific Cav1 knockout male mice are hyperlipidemic regardless of diet but retain endothelial cell function. We found these mice have significantly increased NO in response to the lack of Cav1, and the presence or absence of NO toggled inversely EC lipid content and plasma lipid in mice. The NO nitrosated the fatty acid translocase CD36 at the same cysteines that are palmitoylated on CD36. The nitrosation of CD36 prevented its trafficking to the plasma membrane and decreased lipid accumulation. The physiological effect of this mechanism was a reliance on NO for endothelial function and not dilation.
conclusionsThis work suggests that CD36 nitrosation occurs as a protective mechanism to prevent EC lipotoxicity.
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